Influence of Vitamin C Supplementation on Oxidative Stress and Neutrophil Inflammatory Response in Acute and Regular Exercise

Exercise induces a multitude of physiological and biochemical changes in blood affecting its redox status. Tissue damage resulting fromexercise induces activation of inflammatory cells followed by the increased activity ofmyeloperoxidase (MPO) in circulation. Vitamin C readily scavenges free radicals and may thereby prevent oxidative damage of important biological macromolecules. The aimof this study was to examine the effect of vitamin C supplementation on oxidative stress and neutrophil inflammatory response induced by acute and regular exercise. Experiment was conducted on acute exercise group (performing Bruce Treadmill Protocol (BTP)) and regular training group. Markers of lipid peroxidation, malondialdehyde (MDA), MPO activity, and vitamin C status were estimated at rest and after BTP (acute exercise group) and before and after vitamin C supplementation in both groups. Our results showed increased postexercise Asc in serum independently of vitamin supplementation. They also showed that vitamin C can significantly decrease postexercise MDA level in both experimental groups. Increased postexercise MPO activity has been found in both groups and was not affected by vitamin C supplementation. We concluded that vitamin C supplementation can suppress lipid peroxidation process during exercise but cannot affect neutrophil inflammatory response in either exercise group

EFFECT OF PHYSICAL EXERCISE ON LIPID PEROXIDATION AND ANTIOXIDANT ASCORBIC ACID DEFENSE

Strenuous exercises greatly increase oxygen consumption in the whole body, especially in skeletal muscles. Large part of oxygen consumption is reduced to H2O and ATP, but smaller part (2-5%) results in an increased leakage of electrons from the mitochondrial respiratory chain, forming various reactive oxygen species ─ ROS (O2˙¯, H2O2 i OH˙). These free radicals are capable of triggering a chain of damaging biochemical and physiological reactions (oxidative stress, lipid peroxidation),as a base for skeletal muscles damage after exercise. MDA (malondialdehide) is a marker of exercise induced lipid peroxidation process. L–ascorbic acid is a major aqueous-phase antioxidant. To estimate antioxidant role of ascorbic acid we use rate between dehidroascorbate and ascorbate. In this paper those markers were determinated in 30 students, in rest and after treadmill running protocol (Bruce Treadmill Protocol). It was found that after the treadmill test , plasma MDA level had increased from 3,04 to 4,39 μM/L. Plasma ascorbic acid was also found to be higher after the treadmill test comparing to rest level (from 55,4 to 67,6 μM/L). DHA/A level in rest was 1,62 and after treadmill test it increased to 2,05. These results suggests that strenuous exercise increased process of lipid peroxidation, but in the same time increased ascorbic acid level in plasma and DHA/A rate indicates stronger antioxidant defense system

The Monitoring of Protein Markers of Inflammation and Serum Lipid Concentration in Obese Subjects with Metabolic Syndrome

Background: Obesity is one of the most common modern health problems worldwide. Proinflammatory cells accumulate in the adipose tissue of the obese, and the presence of a low level chronic inflammation in obesity is associated with the emergence of a range of metabolic disorders in cluding cardiovascular disease, insulin resistance, type-2 diabetes, fatty-liver disease, and others. Neutrophils are early parti - cipants in inflammatory processes. After the appropriate stimu lation, these cells release reactive oxygen and nitrogen species, which leads to degranulation and secretion of myeloperoxidase and other enzymes. Myelo per oxidase and its reactive oxidants contribute to tissue damage during inflammatory processes in the human body. Methods: The study included 175 subjects who were, in com - pliance with the International Diabetes Federation criteria, divided into 3 groups: normal weight subjects (N=106), subjects with abdominal obesity (N=37) and the third group consisted of subjects with the metabolic syndrome (N=32). Results: By analyzing the myeloperoxidase enzyme activity (kU/L), and the levels of high-sensitivity C-reactive protein in the blood of all subjects, we detected their significantly higher activity and levels in subjects with the metabolic syndrome, as compared to normal weight subjects (p<0.001). Conclusion: Based on our results, we can conclude that the MPO activity in the serum progressively increases with obesity and the metabolic syndrome, which indicates that this prooxidant enzyme may play a role in the pathophysiological mechanisms of the obesity and the metabolic syndrome related complications

Reduced glutathione level and gsh-dependent enzyme activities in corticonuclear blocks of lenses in patients with senile cataract

Introduction. Reduced compound glutathione (GSH) in the lens has the function to protect the thiol group of lens proteins, and as a substrate of glutathione peroxidase (GPx) and glutathione S-transferase (GST). Protein containing thiol groups is significant for the normal function of lens epithelium, i.e. enzymes Na-K-ATP-ase, thus influencing cell permeability. The relationship GSH/GSSG (oxidized glutathione) is normally high in the lens and other ocular tissue owing to the glutathioneredox cycle, which is localized in the lens epithelium and cortex surface. Objective. The aim of the study was to investigate non-enzymic factors of the antioxidant protection of non-protein and protein tiol, as well as to determine glutathione-dependent enzyme activity in the corticonuclear blocks of lenses in patients with senile cataract. Methods. Biochemical studies of lens were carried on 101 patients with senile cataract. According to cataract maturity degree, the patients were classified into two groups: senile incipient cataract (N=41) and mature senile cataract (N=60). GSH concentration was determined by Ellman’s reagent. GPx activity was assayed with cumene hydroperoxide, and that of glutathione S-transferase by follow-up of glutathione conjugation and 1-chloro-2.4-dinitrobenzene rates. Results. A significantly higher GSH concentration was found in the corticonuclear blocks of lenses with initial as related to mature cataract (p&lt;0.001). The activity of enzyme GPx and GST was considerably higher in the corticonuclear blocks of lenses with initial cataract (p&lt;0.001). With cataract progression, the quantity of available GSH, necessary for GPx and GST functioning, declined, so that the activity of these enzymes was also significantly decreased in mature cataract. Conclusion. The determined lower GSH concentration and antioxidant enzyme activity in corticonuclear blocks of lenses, particularly in cataract with a nuclear component, indicate the weakened antioxidant response of lens tissue during the development of senile cataract

Tacrolimus-induced optic neuropathy: A case report

Intrduction. Tacrolimus (fujimycin or FK506) is a potent immunosuppressive drug with growing usage. It is usually used in prevention of transplanted organ rejection. Its use is highly valuable, but like other immunosupressants, it has adverse effects. One of them is optic neuropathy. Case report. A 47-year-old white male patients who had received tacrolimus therapy for nine years, after kidney transplantation, developed a subacute, painless vision loss on both eyes. He was thoroughly examined on different possible optic neuropathies and other causes of vision loss. After exclusion of other possible causes, the diagnosis of toxic optic neuropathy was established. His therapy was converted to cyclosporine, by his nephrologist, but his vision had improved only slightly. Conclusion. Toxic optic neuropathies are presented in everyday ophthalmological practice, but they are underestimated. Diagnosis can be demanding, especially when it comes to drugs and substances whose possible toxic effect on the optic nerve is not widely known. Unlike other adverse effects of tacrolimus therapy on nervous system, optic neuropathy can causes great and permanent functional impairment

Examination of myeloperoxidase activity, as an indicator of inflammation in obese participants with metabolic syndrome

Introduction. Obesity is a complex metabolic disorder and one of the most common modern health problems. Numerous studies indicate association between chronic low-grade inflammatory state and obesity. Myeloperoxidase (MPO) and its reactive oxidants participate in tissue damage in the course of inflammatory processes. The aim of this study was to examine MPO activity in the serum of obese participants with metabolic syndrome and its relationship with other indicators of inflammation. Material and Methods: Participants were divided into three groups according to the anthropometric parameters and biochemical indicators: normally fed ones (n=30), participants with abdominal obesity (n = 30) and participants with metabolic syndrome (n = 30). In the serum of patients was being determined chlorination activity of MPO by spectrophotometry. Results: Significant differences were found in MPO activity in all three groups of participants such as: the maximum activity was measured in patients with metabolic syndrome (p <0.001). There was a positive correlation between MPO activity and atherogenic index, as well as between the MPO and the concentration of LDL-cholesterol, while the negative correlation was found between MPO and the concentration of HDL-cholesterol. Conclusion: The examination has shown that the activity of MPO progressively increases with obesity and metabolic syndrome. The obtained results suggest that MPO can be of great importance for the pathophysiological mechanisms leading to the development of complications of obesity and metabolic syndrome

Real world experience with nintedanib in connective tissue disease-related interstitial lung disease: a retrospective cohort study

Various connective tissue diseases tend to affect specific organs, lungs being the organ with the most serious repercussions and consequences. The diagnosis of interstitial lung disease makes the treatment more difficult and worsens long-term prognosis and overall survival. Positive results from the registration studies of nintedanib led to approval of the drug for the treatment of idiopathic pulmonary fibrosis and chronic fibrosing interstitial lung diseases in connective tissue diseases. After registration, real-world data on the use of nintedanib are being collected in everyday clinical practise. The objective of the study was to collect and analyse real world experience gathered after the registration of nintedanib for the treatment of CTD-ILD and to show if the positive results collected from a homogeneous and “representative” study population can be applied to everyday clinical practice. We are presenting a retrospective observational case-series study of patients treated with nintedanib from the three largest Croatian centers specialised in the treatment of connective tissue diseases with interstitial lung diseases. Stabilisation or improved of lung function tests was reported in 68% of patients when changes in predicted FVC were observed and in 72% of patients when changes in DLco were analysed. Almost all of the reported patients (98%) were treated with nintedanib as an add-on drug to immunosuppressants. The most common side-effects were gastrointestinal symptoms and abnormal liver function tests in less extent. Our real-world data confirm the tolerability, efficacy and similar side-effects of nintedanib as reported in pivotal trials. Key Points • Interstitial lung disease is a common manifestation of several connective tissue diseases and its progressive fibrosing phenotype contributes to high mortality rate and many unmet needs regarding the treatment remain. • Registration studies of nintedanib obtained sufficient data and positive results to support approval of the drug. • Real-world evidence from our CTD-ILD centres confirm the clinical trial data regarding efficacy, tolerability and safety of nintedanib

Krimska Kongo hemoragijska groznica: prikaz porodičnih epidemija

Uvod. Krimska Kongo hemoragijska groznica (KKHG) je akutna, virusna,prirodno-žarišna zoonoza, koja se u prirodnim uslovima prenosi na čovekaubodom nekih vrsta iksoidnih krpelja i interhumano. Klinički se ispoljavafebrilnim toksično-infektivnim sindromom sa izraženim hemoragijamarazličitih lokalizacija i intenziteta.U radu su prikazani bolesnici lečeni odKrimske-Kongo hemoragijske groznice u Klinici za infektivne bolesti Kliničkobolničkog centra u Prištini.Prikazi porodičnih epidemija. U toku lečenja bolesnika obolelih od KKHGzabeleženo je 6 porodičnih epidemija. U četiri su obolela po dva člana porodice,u jednoj četiri i u jednoj šest članova. Bolest se manifestovala visokomtemperaturom i hemoragijama različitih lokalizacija. U porodičnoj epidemijiu kojoj je obolelo šest članova, kao i u epidemiji u kojoj su obolela četiri člana,letalni ishodi su zabeleženi kod indeksnih bolesnika. Dijagnoza je postavljenana osnovu epidemioloških parametara, kliničke slike i seroloških analiza.Zaključak. Krimsku Kongo hemoragijsku groznicu karakteriše pojava febrilnostii hemoragija, a javlja se sporadično ili u manjim, najčešće porodičnimepidemijama. Od velikog je epidemiološkog značaja mogućnost interhumanetransmisije

The Role of Oxidative Stress in the Onset and Development of Age-Related Macular Degeneration

Age-related macular degeneration (AMD) is a complex, degenerative and progressive chronic disease that leads to severe visual loss. The prevalence of early AMD accounts for 18% in the population between 65 and 74 years of age and even 30% in subjects older than 74 years. The articles published in the last decade point out to a significant role of oxidative stress in the onset and development of age-related macular degeneration. Generally, reactive oxygen species (ROS) are produced in the eye during light absorption and physiological metabolic processes. The level of oxidative stress is kept under control by the action of antioxidants and reparative enzymes. Excessive synthesis of ROS leads to increased oxidative modification of lipids, proteins and DNA, causing oxidative damage of cytoplasmic and nuclear cell elements and changes of the extracellular matrix. The accumulation of oxidatively modified compounds in drusen deposits will initiate the onset and development of AMD. The objective of this review was to highlight the mechanisms of oxidative stress in order to elucidate their significance and association with the pathogenesis of AMD